CNS Flashcards
Hallmark of severe brain injury
Loss of sonsciousness for six or more hours
Causes of focal brain injury
Lesions, edema, coup and contrecoup injury (contusions)
EDH
85% arterial (middle meningeal artery) 15% venous / dural sinus 90% due to skull fracture Temporal fossa is the most common location Earliest symptom is HA
SDH
50% due to skull gractures. Mostly due to bridging veins from torque to the brain
Types of SDH
Acute- Develops within 48 hours of injury and is often located at the top of skull (near bridging veins)
Chronic- develops over weeks to months. Causes chronic HA and tenderness at site. Common in alcoholics.
ICH
Associated with MVA and falls
The hemorrhage acts as an expanding mass. Causes compression of brain tissue with edema
Causes of DAI
AXONAL DAMAGE due to shearing, stretching, or tearing of nerve fibers from shaking, acceleration / deceleration injury, inertial injury
Severity depends on the amount of shearing force applied to brain and brainstem
Grades of Concussion
Grade I- confusion, disorientation, and momentary amnesia
Grade II- momentary confusion and retrograde amnesia
Grade III- confusion with anterograde and retrograde amnesia
Classic Cerebral Concussion
Grade IV
Disconnection of the cerebrum from the brainstem and RAS, causing unconsciousness (<6 hours), anterograde and retrograde amnesia, physiologic and neurologic dysfunction (but ANS still intact).
Types of classic concussion
Complicated (focal injury)
Uncomplicated (no focal injury)
Where is our memory forming system located?
The hippocampus
Postconcussive syndrome symptoms and treatment
HA, cognitive impairments, psychologic and somatic complaints, cranial nerve deficits
Treatment- Reassurance and relief of symptoms. Close monitoring for 24 hours to watch for worsening of symptoms.
Location of most spinal cord trauma
Cervical (1,2,4-7)
Thoracic (T1-L2)
These are the most mobile locations of the vertebral column AND where the cord takes up most of the spinal canal. The area is mobile and the cord doesn’t have much space.
Spinal stenosis
Narrowing at the area where the spinal nerve leaves the vertebra. Can cause numbness, pain, or both, similar to hitting your funny bone. The pain is way out of proportion to the injury actually occurring. Difficult to detect by CT and MRI.
Spinal Shock Affects
Lost normal function below level of injury.
Loss of reflexive function (skeletal, bladder, bowerl, sexual, thermal control, and autonomics).
Remember, if you damage the cord, you will lose your sympathetics because they come from T1-L2. PSNS will be unaffected because that is craniosacral outflow.
Neurogenic Shock
LOSS OF SNS
What would happen if you didn’t have any SNS outflow?
- Vasodilation
- Hypotension
- Bradycardia
- Hypothermia
Think about Garmin’s finger story, and how low your BP could go if actual sympathetics were severed.
Autonomic hyperreflexia
Think about the name. Massive, uncompensated cardio response from SNS outflow due to stimulation of sensory receptors below the level of the cord lesion.
Classic Cerebral Concussion
Grade IV
Disconnection of the cerebrum from the brainstem and RAS, causing unconsciousness (<6 hours), anterograde and retrograde amnesia, physiologic and neurologic dysfunction (but ANS still intact).
Types of classic concussion
Complicated (focal injury)
Uncomplicated (no focal injury)
Where is our memory forming system located?
The hippocampus
Postconcussive syndrome symptoms and treatment
HA, cognitive impairments, psychologic and somatic complaints, cranial nerve deficits
Treatment- Reassurance and relief of symptoms. Close monitoring for 24 hours to watch for worsening of symptoms.
Location of most spinal cord trauma
Cervical (1,2,4-7)
Thoracic (T1-L2)
These are the most mobile locations of the vertebral column AND where the cord takes up most of the spinal canal. The area is mobile and the cord doesn’t have much space.
Spinal stenosis
Narrowing at the area where the spinal nerve leaves the vertebra. Can cause numbness, pain, or both, similar to hitting your funny bone. The pain is way out of proportion to the injury actually occurring. Difficult to detect by CT and MRI.
Spinal Shock Affects
Lost normal function below level of injury.
Loss of reflexive function (skeletal, bladder, bowerl, sexual, thermal control, and autonomics).
Remember, if you damage the cord, you will lose your sympathetics because they come from T1-L2. PSNS will be unaffected because that is craniosacral outflow.
Neurogenic Shock
LOSS OF SNS
What would happen if you didn’t have any SNS outflow?
- Vasodilation
- Hypotension
- Bradycardia
- Hypothermia
Think about Garmin’s finger story, and how low your BP could go if actual sympathetics were severed.
Autonomic hyperreflexia
Think about the name. Massive, uncompensated cardio response from SNS outflow due to stimulation of sensory receptors below the level of the cord lesion.
Why do neurons take forever to re-grow?
Because they are often feet in length and products for repair are only made in the cell body. Products travel at a rate of about 4mm/day.
Why don’t injured axons in the spinal cord regrow?
Because scar tissue develops before the axons can grow. To avoid this, we can induce hyperthermia to suppress the immune system from entering the site and causing scar-tissue to form.
Where may cord swelling be life threatening?
Cervical spine
Where do we get many clots that embolize to the brain?
DVT, carotid artery, or left atrium
What is papilledema?
Edema of the retina
These proteins are associated with higher risk of stroke
Lipoprotein A and homocystein
What is a mycotic aneurysm?
An aneurysm resulting from a bacterial infection of the arterial wall
Examples of vascular malformations
Cavernous angioma
Venous angioma
Capillary telangiectasis
AVM
Do we get cancers of the neurons?
No, because neurons are not mitotic
Brain cells that are responsible for most brain cancers
Glial cells (except the microglia, because these are macrophages, and macrophages do not divide)
Primary intracerebral tumors (gliomas of the CNS)
Astrocytomas (lead to GBM)
Oligodendroglioma
Ependymomas
Primary extracerebral tumors (in the PNS)
Meningioma
Nerve sheath tumors
Metastatic carcinoma
Symptoms of brain tumors/ IICP
Decreased cognition, HA, vomiting, seizures, balance issues, papilledema, loss of sphincter control
Problems with speech and walking are very sensitive to brain problems because they are complicated acts
What is papilledema?
Edema of the retina
What is syringomyelic syndrome?
Inflammation of the spinal cord
Most brain tumors (are/are not) metastatic
Are not
Types of meningitis
Bacteria
Aseptic (viral)
Fungal
TB
Neurologic complications of AIDS
Neuropathy, cognitive dysfunction, opportunistic meningitis infections, neoplasms, myelopathy (spinal cord pathology), and neuropathy
Conditions cause by brain degeneration
Alzheimers Parkinson's Huntington's ALS MS Guillain-Barre MG Poliomyelitis
Classifications of dementia
Cortical - Alzheimer's and Pick's disease Subcortical - Parkinson and huntington Cortical and subcortical - Infection and CJD
Parkinson Dementia
50% have depression
50% excessive daytime sleepiness
Disorientation, confusion, punding, memory loss, distractibility, and difficulty with concept formation, abstraction, calculations, thinking, and judgement
Symptoms will fluctuate, but progressively worsen
What is punding?
Intense fascination with repetitive handling and examining of mechanical objects
Cause of Huntington’s
Hereditary (Autosomal dominant)
Severe degeneration of the basal ganglia (caudate and putamen) and frontal cortex. Depletion of GABA.
Symptoms of Huntington’s
Choreiform movements and disturbed thought processes
Consequences of seizures
250% increase in brain ATP consumption
250% increase in CBF
60% increase in brain O2 consumption
Available glucose and oxygen are depleted. Lactate accumulates in brain tissue. May result in progressive brain tissue injury due to cellular exhaustion and destruction.
ALS
Causes progressive weakness leading to resp failure and death. Normal cognition until death.
Think of Stephen Hawking.
Guillain Barre Syndrome
Ascending motor paralysis. Inflammatory disease caused by demyelination of peripheral nerves.
Often triggered by a stomach flu *****
MG Cause
IgG produced against ACh receptors. Hallmark is weakness that progresses with use
What happens during a myasthenic crisis?
Can’t breath
What causes coma?
Damage to bilateral hemispheres
Damage to the RAS
Why are pupils diagnostic?
Because contracting pupils is a complex process. Depending on what happens to the pupils will hint where the damage is located.
Cerebral death causes
Persistant vegetative state. Can also progress into a minimal conscious state such as akinetic mutism or locked-in syndrome
What is status epilepticus?
Sustained seizure for more than 30 minutes. Also can be a second seizure that begins before a person regains consciousness from their first one.
Consequences of seizures
250% increase in brain ATP consumption
250% increase in CBF
60% increase in brain O2 consumption
Types of cerebral edema
Vasogenic
Cytotoxic
Ischemic
Interstitial
Causes of hydrocephalus
Decreased reabsorption (damage to arachnoid granulations) Increased fluid production (tumor of choroid plexus) Obstruction within ventricular system
Normal hydrocephalus
Hydro without IICP.
May be caused in conditions such as Huntington’s, where you are losing brain material and i is replaced by CSF. Here you have more CSF than normal, but it is not causing pressure
Biggest risk factors of having a CVA
Smoking, age, and HTN
Cause of MG
IgG produced against ACh receptors
